The Brain-Gut Team.

BACKGROUND: Interactions between brain and gut have been suspected for centuries but our understanding of the neural centers and neurohormonal links that establish bidirectional regulatory communication between these 2 body systems has advanced significantly in the last decades. The label "brain-gut axis" designates a useful but deceivingly simple concept, since the mechanistic complexity of brain-gut interaction is enormous. SUMMARY: The significance of the brain-gut axis is perhaps best conceived as "a team" since both systems are physiologically coordinated to ensure a healthy status. However, under pathophysiological conditions, the axis also contributes substantially to distort homeostasis. For instance, normal signals emanating from the gut may be inappropriately received and interpreted by the central nervous system that responds by inadequately recruiting other brain structures and generate both symptoms and commands that disturb normal gut activity. Key Messages: Thus, at each end and in the brain-gut connecting routes, there is the potential for altering perceived and unperceived sensations and further impinging on normal function.

Enteric neuron density correlates with clinical features of severe gut dysmotility.

Gastrointestinal (GI) symptoms can originate from severe dysmotility due to enteric neuropathies. Current methods used to demonstrate enteric neuropathies are based mainly on classic qualitative histopathological/immunohistochemical evaluation. This study was designed to identify an objective morphometric method for paraffin-embedded tissue samples to quantify the interganglionic distance between neighboring myenteric ganglia immunoreactive for neuron-specific enolase, as well as the number of myenteric and submucosal neuronal cell bodies/ganglion in jejunal specimens of patients with severe GI dysmotility. Jejunal full-thickness biopsies were collected from 32 patients (22 females; 16-77 yr) with well-characterized severe dysmotility and 8 controls (4 females; 47-73 yr). A symptom questionnaire was filled before surgery. Mann-Whitney U test, Kruskal-Wallis coupled with Dunn's posttest and nonparametric linear regression tests were used for analyzing morphometric data and clinical correlations, respectively. Compared with controls, patients with severe dysmotility exhibited a significant increase in myenteric interganglionic distance (P = 0.0005) along with a decrease in the number of myenteric (P < 0.00001) and submucosal (P < 0.0004) neurons. A 50% reduction in the number of submucosal and myenteric neurons correlated with an increased interganglionic distance and severity of dysmotility. Our study proposes a relatively simple tool that can be applied for quantitative evaluation of paraffin sections from patients with severe dysmotility. The finding of an increased interganglionic distance may aid diagnosis and limit the direct quantitative analysis of neurons per ganglion in patients with an interganglionic distance within the control range.NEW & NOTEWORTHY Enteric neuropathies are challenging conditions characterized by a severe impairment of gut physiology, including motility. An accurate, unambiguous assessment of enteric neurons provided by quantitative analysis of routine paraffin sections may help to define neuropathy-related gut dysmotility. We showed that patients with severe gut dysmotility exhibited an increased interganglionic distance associated with a decreased number of myenteric and submucosal neurons, which correlated with symptoms and clinical manifestations of deranged intestinal motility.

Gut epithelial and vascular barrier abnormalities in patients with chronic intestinal pseudo-obstruction.

BACKGROUND: Chronic intestinal pseudo-obstruction (CIPO) is a rare condition due to severe impairment of gut motility responsible for recurrent subocclusive episodes. Although neuromuscular-glial-ICC abnormalities represent the main pathogenetic mechanism, the pathophysiology of CIPO remains poorly understood. Intestinal epithelial and vascular endothelial barrier (IEVB) abnormalities can contribute to neuroepithelial changes by allowing passage of harmful substances. METHODS: To test retrospectively whether IEVB defects occur in patients with CIPO, we measured the jejunal protein expression of the major tight junction (TJ) components. CIPO patients were subdivided according to gut neuromuscular histopathology: apparently normal (AN); with inflammation (INF); or with degenerative alterations (DEG). The presence of occludin/claudin oligomers (index of TJ assembly), the amount of occludin, claudin-4, and zonula occludens-1 (ZO-1), and the expression of vasoactive intestinal polypeptide (VIP) and glial fibrillary acidic protein (GFAP) immunoreactivities were evaluated on jejunal full-thickness biopsies using Western blot. KEY RESULTS: Oligomers were absent in the 73% of CIPO. Total occludin decreased in CIPO with AN and INF changes. Claudin-4 was upregulated in CIPO with INF and DEG features. ZO-1 and VIP expression decreased selectively in DEG group. GFAP increased in CIPO regardless the histopathological phenotype. CONCLUSIONS & INFERENCES: The absence of oligomers demonstrated in our study suggests that IEBV is altered in CIPO. The mechanism leading to oligomerization is occludin-dependent in AN and INF, whereas is ZO-1-dependent in DEG. Our study provides support to IEVB abnormalities contributing to CIPO clinical and histopathological features.

Bloating and Abdominal Distension: Old Misconceptions and Current Knowledge.

Bloating, as a symptom and abdominal distension, as a sign, are both common functional-type complaints and challenging to manage effectively. Individual patients may weight differently the impact of bloating and distension on their well-being. Complaints may range from chronic highly distressing pain to simply annoying and unfashionable protrusion of the abdomen. To avoid mishaps, organic bloating, and distension should always be considered first and appropriated assessed. Functional bloating and distension often present in association with other manifestations of irritable bowel syndrome or functional dyspepsia and in that context patients tend to regard them as most troublesome. A mechanism-based management bloating and distension should be ideal but elucidating key operational mechanisms in individual patients is not always feasible. Some clues may be gathered through a detailed dietary history, by assessing bowel movement frequency and stool consistency and special imaging technique to measure abdominal shape during episodes of distension. In severe, protracted cases it may be appropriate to refer the patient to a specialized center where motility, visceral sensitivity, and abdominal muscle activity in response to intraluminal stimuli may be measured. Therapeutic resources focussed upon presumed or demonstrated pathogenetic mechanism include dietary modification, microbiome modulation, promoting gas evacuation, attenuating visceral perception, and controlling abdominal wall muscle activity via biofeedback.

Small Bowel Motility.

PURPOSE OF REVIEW: Small bowel motility disorders constitute a relatively small but important segment of clinical gastroenterology. Presenting features encompass a broad range of symptom manifestations and severity: from chronic functional-type complaints to life-threatening nutritional impairment. Diagnostic assessment of patients with suspected intestinal motility disorders is often hampered by the complexity of measuring intestinal contractile activity in humans. In this review, we describe and critically comment the main current and forthcoming methodologies. RECENT FINDINGS: Beyond conventional small bowel manometry, radiological methods, and intestinal transit tests that have been available for several decades, now we focus on novel methodologies such as high-resolution manometry, magnetic resonance methodology, and endoluminal capsule image analysis. Gradual introduction of new approaches to diagnostic investigation of patients with suspected intestinal motility disorders should facilitate a less invasive and more accurate characterization of disturbed motor function. Enhanced understanding of the pathophysiological basis of clinical conditions should allow better application of therapeutic approaches that are also highlighted in this review.

Effect of prucalopride on intestinal gas tolerance in patients with functional bowel disorders and constipation.

BACKGROUND AND AIM: Patients with functional bowel disorders develop gas retention and symptoms in response to intestinal gas loads that are well tolerated by healthy subjects. Stimulation of 5HT-4 receptors in the gut has both prokinetic and antinociceptive effects. The aim of this study is to determine the effect of prucalopride, a highly selective 5HT-4 agonist, on gas transit and tolerance in women with functional bowel disorders complaining of constipation. METHODS: Twenty-four women with functional bowel disorders complaining of constipation were included in the study. Patients were studied twice on separate days in a cross-over design. On each study day, an intestinal gas challenge test was performed. During the five previous days, prucalopride (2 mg/day) or placebo was administered. Abdominal symptoms, stool frequency, and stool consistency were recorded during the treatment period on daily questionnaires. RESULTS: During the gas challenge test, prucalopride did not decrease the volume of gas retained in the subset of patients who had significant gas retention (≥ 200 mL) while on placebo. However, in those patients who had increased symptoms during the gas test (≥ 3 on a 0 to 6 scale) when on placebo, prucalopride did significantly reduce the perception of symptoms (2.3 ± 0.5 mean score vs 3.5 ± 0.3 on placebo; P = 0.045). During the treatment period with prucalopride, patients exhibited an increase in the total number of bowel movements and decreased stool consistency compared with placebo. CONCLUSION: Prucalopride reduces abdominal symptoms without modifying gas retention when patients with functional bowel disorders are challenged with the gas transit and tolerance test. European Clinical Trials Database (EudraCT2011-006354-86).

Gastroduodenal Disorders.

Symptoms that can be attributed to the gastroduodenal region represent one of the main subgroups among functional gastrointestinal disorders. A slightly modified classification into the following 4 categories is proposed: (1) functional dyspepsia, characterized by 1 or more of the following: postprandial fullness, early satiation, epigastric pain, and epigastric burning, which are unexplained after a routine clinical evaluation; and includes 2 subcategories: postprandial distress syndrome that is characterized by meal-induced dyspeptic symptoms and epigastric pain syndrome that does not occur exclusively postprandially; the 2 subgroups can overlap; (2) belching disorders, defined as audible escapes of air from the esophagus or the stomach, are classified into 2 subcategories, depending on the origin of the refluxed gas as detected by intraluminal impedance measurement belching: gastric and supragastric belch; (3) nausea and vomiting disorders, which include 3 subcategories: chronic nausea and vomiting syndrome; cyclic vomiting syndrome; and cannabinoid hyperemesis syndrome; and (4) rumination syndrome.

Mechanism-Oriented Therapy of Irritable Bowel Syndrome.

Irritable bowel syndrome (IBS) is a common and well-accepted diagnosis but often imprecisely applied to patients in usual clinical practice. Diagnosis is entirely based on symptom criteria that tend to include broad strata of abdominal complainers. Established criteria for diagnosis are strictly followed in controlled clinical trials for new therapeutic agents, but physicians are more lax in the clinic. Predictably, in light of the above ambiguities, many pathogenetic mechanisms and pathophysiological disturbances appear to be involved in IBS, but so far no mechanism-based subgroupings to guide specific therapy have been soundly established. Thus, diverse therapeutic approaches coexist and are discretionally prescribed by attending clinicians on the basis of major manifestations (i.e., diarrhea-predominance or constipation-predominance), more or less apparent psychological disturbances, and patient preferences (pharmacological versus dietary or microbiological approaches). In this review, we have attempted to update scientific knowledge about the more relevant disease mechanisms involved and relate this more fundamental basis to the various treatment options available today.

Randomized, Placebo-Controlled Trial of Biofeedback for the Treatment of Rumination.

OBJECTIVES: We previously demonstrated that rumination is produced by an unperceived, somatic response to food ingestion, and we developed an original biofeedback technique based on electromyography (EMG)-guided control of abdomino-thoracic muscular activity. Our aim was to demonstrate the superiority of biofeedback vs. placebo for the treatment of rumination. METHODS: Randomized, placebo-controlled trial performed in a referral center. Consecutive patients who fulfilled the Rome III criteria for rumination (18 women, 6 men; 19-79 years age) were selected and all included in the study; 1 patient assigned to placebo withdrew because of an unrelated accident. Abdomino-thoracic muscle activity after a challenge meal was recorded by EMG. The patients in the biofeedback group were shown the signal and instructed to control muscle activity, whereas the patients in the placebo group were not shown the signal and were given oral simethicone. Each patient underwent 3 sessions over a 10-day period. MAIN OUTCOME: number of rumination events as measured by questionnaires for 10 consecutive days before and after intervention. RESULTS: Patients on biofeedback (n=12) but not on placebo (n=11) effectively learned to reduce intercostal activity (by 51±6% vs. 10±7% increment on placebo; P<0.001) and anterior wall muscle activity (by 52±4% vs. 9±2% increment on placebo; P<0.001). Biofeedback treatment resulted in a 74±6% reduction in rumination activity (from 29±6 before to 7±2 daily events after intervention) vs. 1±14% on placebo; P=0.001 (from 21±2 before to 21±4 daily events after intervention). CONCLUSIONS: Rumination can be effectively corrected by biofeedback-guided control of abdomino-thoracic muscular activity.

Effect of selective CCK1 receptor antagonism on accommodation and tolerance of intestinal gas in functional gut disorders.

BACKGROUND: Participants with functional gut disorders develop gas retention and symptoms in response to intestinal gas loads that are well tolerated by healthy subjects. To determine the role of cholecystokinin (CCK1 ) receptors on gas transit and tolerance in women with functional gut disorders. METHODS: In 12 healthy women, and 24 women with functional gut disorders (12 dyspepsia and 12 constipation-predominant irritable bowel syndrome) gas was infused into the jejunum at 12 mL/min for 3 h with simultaneous duodenal lipid infusion (intralipid 1 kcal/min), while measuring anal gas evacuation and abdominal symptoms on a 0-6 score scale. Triple-blind paired studies during iv infusion of dexloxiglumide (2.5 mg/kg bolus plus 5 mg/kg h continuous infusion), a selective CCK1 inhibitor, or saline (control) were performed in random order. RESULTS: During saline infusion participants with functional gut disorders developed significantly greater gas retention and abdominal symptoms than healthy subjects (394 ± 40 mL vs 265 ± 35 mL and 2.8 ± 0.3 vs 1.9 ± 0.4 highest abdominal symptom score, respectively; P < 0.05 for both). Dexloxiglumide increased gas retention in both groups (514 ± 35 mL and 439 ± 60 mL, respectively; P = 0.033 vs saline for both); however, despite the larger retention, dexloxiglumide reduced abdominal symptoms (2.3 ± 0.2 score and 0.8 ± 0.3 score, respectively; P = 0.05 vs saline for both). Post-hoc analysis showed that, the decrease in abdominal symptoms was more pronounced in those participants with functional gut disorders with higher basal abdominal symptoms than in the rest (P = 0.037). CONCLUSION: Inhibition of CCK1 receptors by dexloxiglumide increases intestinal gas retention and reduces abdominal symptoms in response to by intestinal gas loads. European Clinical Trials Database (EudraCT 2005-003338-16).

Classification of functional bowel disorders by objective physiological criteria based on endoluminal image analysis.

We have previously developed an original method to evaluate small bowel motor function based on computer vision analysis of endoluminal images obtained by capsule endoscopy. Our aim was to demonstrate intestinal motor abnormalities in patients with functional bowel disorders by endoluminal vision analysis. Patients with functional bowel disorders (n = 205) and healthy subjects (n = 136) ingested the endoscopic capsule (Pillcam-SB2, Given-Imaging) after overnight fast and 45 min after gastric exit of the capsule a liquid meal (300 ml, 1 kcal/ml) was administered. Endoluminal image analysis was performed by computer vision and machine learning techniques to define the normal range and to identify clusters of abnormal function. After training the algorithm, we used 196 patients and 48 healthy subjects, completely naive, as test set. In the test set, 51 patients (26%) were detected outside the normal range (P < 0.001 vs. 3 healthy subjects) and clustered into hypo- and hyperdynamic subgroups compared with healthy subjects. Patients with hypodynamic behavior (n = 38) exhibited less luminal closure sequences (41 ± 2% of the recording time vs. 61 ± 2%; P < 0.001) and more static sequences (38 ± 3 vs. 20 ± 2%; P < 0.001); in contrast, patients with hyperdynamic behavior (n = 13) had an increased proportion of luminal closure sequences (73 ± 4 vs. 61 ± 2%; P = 0.029) and more high-motion sequences (3 ± 1 vs. 0.5 ± 0.1%; P < 0.001). Applying an original methodology, we have developed a novel classification of functional gut disorders based on objective, physiological criteria of small bowel function.

Abdominothoracic mechanisms of functional abdominal distension and correction by biofeedback.

BACKGROUND & AIMS: In patients with functional gut disorders, abdominal distension has been associated with descent of the diaphragm and protrusion of the anterior abdominal wall. We investigated mechanisms of abdominal distension in these patients. METHODS: We performed a prospective study of 45 patients (42 women, 24-71 years old) with functional intestinal disorders (27 with irritable bowel syndrome with constipation, 15 with functional bloating, and 3 with irritable bowel syndrome with alternating bowel habits) and discrete episodes of visible abdominal distension. Subjects were assessed by abdominothoracic computed tomography (n = 39) and electromyography (EMG) of the abdominothoracic wall (n = 32) during basal conditions (without abdominal distension) and during episodes of severe abdominal distension. Fifteen patients received a median of 2 sessions (range, 1-3 sessions) of EMG-guided, respiratory-targeted biofeedback treatment; 11 received 1 control session before treatment. RESULTS: Episodes of abdominal distension were associated with diaphragm contraction (19% ± 3% increase in EMG score and 12 ± 2 mm descent; P < .001 vs basal values) and intercostal contraction (14% ± 3% increase in EMG scores and 6 ± 1 mm increase in thoracic antero-posterior diameter; P < .001 vs basal values). They were also associated with increases in lung volume (501 ± 93 mL; P < .001 vs basal value) and anterior abdominal wall protrusion (32 ± 3 mm increase in girth; P < .001 vs basal). Biofeedback treatment, but not control sessions, reduced the activity of the intercostal muscles (by 19% ± 2%) and the diaphragm (by 18% ± 4%), activated the internal oblique muscles (by 52% ± 13%), and reduced girth (by 25 ± 3 mm) (P ≤ .009 vs pretreatment for all). CONCLUSIONS: In patients with functional gut disorders, abdominal distension is a behavioral response that involves activity of the abdominothoracic wall. This distension can be reduced with EMG-guided, respiratory-targeted biofeedback therapy.

Biofeedback-guided control of abdominothoracic muscular activity reduces regurgitation episodes in patients with rumination.

BACKGROUND & AIMS: Rumination syndrome is characterized by effortless recurrent regurgitation of recently ingested food into the mouth, with consequent expulsion or re-chewing and swallowing. We investigated whether rumination is under volitional control and can be reversed by behavioral treatment. METHODS: We performed a prospective study of 28 patients who fulfilled the Rome criteria for rumination and had no organic disorders on the basis of a thorough evaluation. The diagnosis of rumination was confirmed by intestinal manometry (abdominal compression associated with regurgitation). Patients were trained to modulate abdominothoracic muscle activity under visual control of electromyographic recordings. Recordings were made after challenge meals, before training (baseline), and during 3 treatment sessions. Outcome was measured by questionnaires administered daily for 10 days before training, immediately after training, and at 1, 3, and 6 months after training. RESULTS: By the end of the 3 sessions, patients had effectively learned to reduce intercostal activity (by 50% ± 2%; P < .001 vs basal) and anterior wall muscle activity (by 30% ± 6%; P < .001 vs basal). Patients reported 27 ± 1 regurgitation episodes/day at baseline and 8 ± 2 episodes/day immediately after treatment. Regurgitation episodes decreased further to 4 ± 1 episodes at 6 months after training. CONCLUSIONS: Rumination is produced by an unperceived somatic response to food ingestion that disrupts abdominal accommodation and can be effectively corrected by biofeedback-guided control of abdominothoracic muscular activity.

Mechanisms of postprandial abdominal bloating and distension in functional dyspepsia.

OBJECTIVE: Patients with irritable bowel syndrome and abdominal bloating exhibit abnormal responses of the abdominal wall to colonic gas loads. We hypothesised that in patients with postprandial bloating, ingestion of a meal triggers comparable abdominal wall dyssynergia. Our aim was to characterise abdominal accommodation to a meal in patients with postprandial bloating. DESIGN: A test meal (0.8 kcal/ml nutrients plus 27 g/litre polyethylenglycol 4000) was administered at 50 ml/min as long as tolerated in 10 patients with postprandial bloating (fulfilling Rome III criteria for postprandial distress syndrome) and 12 healthy subjects, while electromyographic (EMG) responses of the anterior wall (upper and lower rectus, external and internal oblique via bipolar surface electrodes) and the diaphragm (via six ring electrodes over an oesophageal tube in the hiatus) were measured. Means +/- SD were calculated. RESULTS: Healthy subjects tolerated a meal volume of 913±308 ml; normal abdominal wall accommodation to the meal consisted of diaphragmatic relaxation (EMG activity decreased by 15±6%) and a compensatory contraction (25±9% increase) of the upper abdominal wall muscles (upper rectus and external oblique), with no changes in the lower anterior muscles (lower rectus and internal oblique). Patients tolerated lower volume loads (604±310 ml; p=0.030 vs healthy subjects) and developed a paradoxical response, that is, diaphragmatic contraction (14±3% EMG increment; p<0.01 vs healthy subjects) and upper anterior wall relaxation (9±4% inhibition; p<0.01 vs healthy subjects). CONCLUSIONS: In functional dyspepsia, postprandial abdominal distension is produced by an abnormal viscerosomatic response to meal ingestion that alters normal abdominal accommodation.

Anal gas evacuation and colonic microbiota in patients with flatulence: effect of diet.

OBJECTIVE: To characterise the influence of diet on abdominal symptoms, anal gas evacuation, intestinal gas distribution and colonic microbiota in patients complaining of flatulence. DESIGN: Patients complaining of flatulence (n=30) and healthy subjects (n=20) were instructed to follow their usual diet for 3 days (basal phase) and to consume a high-flatulogenic diet for another 3 days (challenge phase). RESULTS: During basal phase, patients recorded more abdominal symptoms than healthy subjects in daily questionnaires (5.8±0.3 vs 0.4±0.2 mean discomfort/pain score, respectively; p=<0.0001) and more gas evacuations by an event marker (21.9±2.8 vs 7.4±1.0 daytime evacuations, respectively; p=0.0001), without differences in the volume of gas evacuated after a standard meal (262±22 and 265±25 mL, respectively). On flatulogenic diet, both groups recorded more abdominal symptoms (7.9±0.3 and 2.8±0.4 discomfort/pain, respectively), number of gas evacuations (44.4±5.3 and 21.7±2.9 daytime evacuations, respectively) and had more gas production (656±52 and 673±78 mL, respectively; p<0.05 vs basal diet for all). When challenged with flatulogenic diet, patients' microbiota developed instability in composition, exhibiting variations in the main phyla and reduction of microbial diversity, whereas healthy subjects' microbiota were stable. Taxa from Bacteroides fragilis or Bilophila wadsworthia correlated with number of gas evacuations or volume of gas evacuated, respectively. CONCLUSIONS: Patients complaining of flatulence have a poor tolerance of intestinal gas, which is associated with instability of the microbial ecosystem.

Impact of orocecal transit time on patient´s perception of lactose intolerance.

BACKGROUND: symptoms attributed to the lactose intolerance are an important public health issue because of their prevalence and social relevance. Also because they may cause undue rejection of dairy products consume with potential health consequences. Transit time is a putative factor implied in the severity of symptoms associated with lactose. OBJECTIVES: to elucidate the relation between orocecal transit time (OCTT) and lactose intolerance symptoms. METHODS: observational study in patients referred to a lactose hydrogen breath test who showed an increase in breath H2 excretion higher than 25 ppm. OCTT was measured with the breath test and symptoms of lactose tolerance with a validated scale. Symptoms were measured twice: before receiving the lactose, inquiring about self perceived symptoms when patients consumed dairy products at home ("home symptoms"), and again after completing the lactose breath test ("test symptoms"). RESULTS: 161 patients were included. There was no correlation between OCTT and home symptoms (r = -0.1). When OCTT was faster than 60 minutes, intensity of "test symptoms" was similar to "home symptoms". However, in patients with normal or slow OCTT, the "home symptoms" were more intense than the "test symptoms" (p < 0.05). At home, symptoms were independent of OCTT but with the lactose test load the symptoms were proportionately more intense with faster OCTT. CONCLUSIONS: in lactose maldigesters, selfreported symptoms of lactose intolerance are more pronounced at home than after a high lactose challenge. Intolerance symptoms that patients attributed to lactose consume at home are due to factors other than fast OCTT.

Influencia del tiempo de tránsito orocecal en la percepción de los síntomas de intolerancia a la lactosa / Impact of orocecal transit time on patient’s perception of lactose intolerance

Antecedentes: los síntomas atribuidos a la intolerancia a la lactosa son un importante problema de salud pública. El tiempo de tránsito es un factor implicado en la severidad de los síntomas asociados al consumo de lactosa. Objetivos: elucidar la relación entre el tiempo de tránsito orocecal (TTOC) y los síntomas de intolerancia a la lactosa. Métodos: estudio observacional en pacientes con un test del aliento de hidrógeno con lactosa patológico (excreción de hidrógeno superior a 25 ppm). El TTOC se midió mediante el test del aliento y los síntomas mediante una escala previamente validada. Los síntomas se determinaron dos veces: antes de recibir la lactosa, preguntando acerca de los síntomas en casa cuando se consumen lácteos (“síntomas en casa”), y de nuevo después de completar el test del aliento con lactosa (“síntomas test”). Resultados: se han incluido 161 pacientes. No se observa correlación entre el TTOC y los síntomas en casa (r = -0,1). Cuando el TTOC fue más rápido de 60 minutos, la intensidad de los “síntomas test” fue parecida a la de los “síntomas en casa”. Sin embargo, en los pacientes con TTOC normal o lento, los “síntomas en casa” fueron más intensos que los “síntomas test” (p < 0,05). En casa los síntomas fueron independientes del TTOC mientras que después de la sobrecarga de lactosa los síntomas fueron más intensos cuanto más rápido el TTOC. Conclusiones: los síntomas que refieren las personas con malabsorción de lactosa son más pronunciados en casa que tras una sobrecarga de lactosa. Los síntomas de intolerancia que los pacientes atribuyen al consumo de lactosa en casa no son debidos a un TTOC rápido(AU)

Background: symptoms attributed to the lactose intolerance are an important public health issue because of their prevalence and social relevance. Also because they may cause undue rejection of dairy products consume with potential health consequences. Transit time is a putative factor implied in the severity of symptoms associated with lactose. Objectives: to elucidate the relation between orocecal transit time (OCTT) and lactose intolerance symptoms. Methods: observational study in patients referred to a lactose hydrogen breath test who showed an increase in breath H2 excretion higher than 25 ppm. OCTT was measured with the breath test and symptoms of lactose tolerance with a validated scale. Symptoms were measured twice: before receiving the lactose, inquiring about self perceived symptoms when patients consumed dairy products at home (“home symptoms”), and again after completing the lactose breath test (“test symptoms”). Results: 161 patients were included. There was no correlation between OCTT and home symptoms (r = -0.1). When OCTT was faster than 60 minutes, intensity of “test symptoms” was similar to “home symptoms”. However, in patients with normal or slow OCTT, the “home symptoms” were more intense than the “test symptoms” (p < 0.05). At home, symptoms were independent of OCTT but with the lactose test load the symptoms were proportionately more intense with faster OCTT. Conclusions: in lactose maldigesters, selfreported symptoms of lactose intolerance are more pronounced at home than after a high lactose challenge. Intolerance symptoms that patients attributed to lactose consume at home are due to factors other than fast OCTT(AU)

Diseases of the digestive tract: is prevention possible and feasible?

Prevention is and will remain a major goal of medicine and gastroenterology. Economics will have a major influence. Preventive approaches will need to prove a favorable cost-benefit ratio before they are authorized for broad implementation. Personalized medicine is just starting, but undoubtedly it will accelerate, gain relevance and become an integral part of our clinical practice. Physicians in general and gastroenterologists specifically will need to seriously contemplate retraining/refocusing to gain competence in genetic/proteomic evaluation of individuals, or risk a significant degree of obsolescence.

Abdomino-phrenic dyssynergia in patients with abdominal bloating and distension.

OBJECTIVES: The abdomen normally accommodates intra-abdominal volume increments. Patients complaining of abdominal distension exhibit abnormal accommodation of colonic gas loads (defective contraction and excessive protrusion of the anterior wall). However, abdominal imaging demonstrated diaphragmatic descent during spontaneous episodes of bloating in patients with functional gut disorders. We aimed to establish the role of the diaphragm in abdominal distension. METHODS: In 20 patients complaining of abdominal bloating and 15 healthy subjects, we increased the volume of the abdominal cavity with a colonic gas load, while measuring abdominal girth and electromyographic activity of the anterior abdominal muscles and of the diaphragm. RESULTS: In healthy subjects, the colonic gas load increased girth, relaxed the diaphragm, and increased anterior wall tone. With the same gas load, patients developed significantly more abdominal distension; this was associated with paradoxical contraction of the diaphragm and relaxation of the internal oblique muscle. CONCLUSIONS: In this experimental provocation model, abnormal accommodation of the diaphragm is involved in abdominal distension.